NYRF(chinese herb)

[Regulative effects of Chinese herbs for nourishing yin and removing fire on gene expressions of estrogen receptor alpha, insulin-like growth factor-1 receptor, epithelial growth factor receptor and protein synthesis in epiphyseal growth plate of female pubertal rats].

"To investigate the effect of Chinese herbs for nourishing yin and removing fire (NYRF) on gene expressions of estrogen receptor alpha (ER alpha), insulin-like growth factor-1 receptor (IGF-1R) and epithelial growth factor receptor (EGFR) in the epiphyseal growth plate of the female pubertal rats.
The rats were randomly divided into the control group and the intervened group. Immunohistochemistry and realtime-PCR methods were used to measure the gene expression of ER alpha, IGF-1R and EGFR and their protein synthesis in epiphyseal growth plate.
After being intervened with NYRF, the gene expressions of ER alpha and IGF-1R were down-regulated and their protein synthesis markedly reduced, while those of EGFR were unchanged.
NYRF can modulate the development and maturation of bone by regulating the expressions of ER alpha and IGF-1R in the epiphyseal growth plate."

ERalpha inhibition may result in increased length but IGF1R knockout reduces height.

[Effect of Chinese herbs for nourishing shen-yin and removing xiang-fire on estrogen receptor expression in reproductive organ of rats contaminated with environmental endocrine disruptor].

"To investigate the effect of Chinese herbs for nourishing Shen-yin and removing Xiang-fire (NYRF) on estrogen receptor (ER) expression in uterus and ovary of rats contaminated with nonylphenol (NP) or its bisphenol A (BPA) mixture, for exploring the action mechanism of NYRF in antagonizing the estrogen-mimetic activity of environmental endocrine disruptors (EEDs).
EEDs contaminated female SD rats, 3-week old, were divided into two groups, the treated group fed with NYRF and the control group with corn oil during the same period of contaminating for 15 days. The wet weight (WW) and organ coefficient (OC) of uterus in rats, as well as the ER protein and mRNA expressions in rat's uterus and ovary were detected and compared.
As compared with normal range, WW and OC increased significantly in the contaminated rats of the control group, with significantly down-regulated ER protein expression in uterus, and expressions of ER alpha and ER beta gene and protein in ovary (P<0.05). While in the treated group, the above-mentioned abnormalities of various indictors were markedly reversed to a certain extent (P<0.05).
EEDs show estrogenic-mimetic action on productive organs, which could be antagonized by NYRF, resulting in the down-regulated mRNA and protein expressions of ER in reproductive organs, so as to reduce the sensibility of reproductive organs to EEDs, which is probably one of the acting mechanisms of NYRF."


Effect of nourishing “Yin”-removing “Fire” Chinese herbal mixture on hypothalamic kisspeptin expression in female precocious rats

"Both male and female rats show an obvious increase in Kiss-1 mRNA levels that coincides with the onset of puberty. Pharmacological analyses further set the contention that kisspeptin is likely the most potent elicitor of the GnRH/gonadotropic axis known so far"

"[YNRF] decreased the expression levels of GnRH, FSH and LH mRNAs in female adolescent rats"

"The mixture prescription is mainly composed of 10 medicinal plants: 15 g of Rehmannia glutinosa (Sheng di), 9 g each of Scrophularia buergeriana (Xuan shen), Anemarrhena asphodeloides (Zhi mu), Cortex Phellodendri (Huang bai), Paeonia suffruticosa Andr. (Dan pi), Alisma plantago-aquatica L. var. orientala Sam (Ze xie), Prunella vulgaris L. (Xia ku cao), 12 g of Carapax et Plastrum Testudinis (Gui jia), 30 g of Fructus hordei germinate (Mai ya) and 6 g of Gentiana scabra Bge. (Long dan cao)."

Included in Le Shu Yuan Jin Yin Hua tea.

Gas1

Gas1 is upregulated by LSJL.


Functions of the growth arrest specific 1 gene in the development of the mouse embryo.

"The growth arrest specific 1 (gas1) gene is highly expressed in quiescent mammalian cells. Overexpression of gas1 in normal could inhibit G(0)/G(1) transition. The spatial-temporal expression patterns for gas1 were established in 8.5- to 14.5-day-old embryos by immunohistochemical staining and in situ hybridization. Gas1 was found heterogeneously expressed in [the] limb. The antiproliferative effects of gas1 on 10.5 and 12.5 day limb cells were investigated by flow cytometry. In 10.5 day limbs cells, gas1 overexpression could not prevent G(0)/G(1) progression.  Gas1 could only induce growth arrest if p53 was also coexpressed {p53 was not coexpressed significantly in LSJL}. In contrast, gas1 overexpression alone was able to induce growth arrest in 12.5 day limb cells. We also examined the cell cycle profile of gas1-expressing and nonexpressing cells by immunochemistry and flow cytometry. For 10.5 day Gas1-expressing limb cells, we did not find these cells preferentially distributed at G0/G1, as compared with Gas1-negative cells. However, in the 12.5 day limb, we did find significantly more Gas1-expressing cells distributed at G0/G1 phase than Gas1-negative cells. Gas1 alone, during the early stages of development, could not inhibit cell growth. This inhibition was only established when the embryo grew older. We have overexpressed gas1 in subconfluent embryonic limb cells to determine the ability of gas1 to cross-talk with various response elements of important transduction pathways. Specifically, we have examined the interaction of gas1 with Ap-1, NFkappaB, and c-myc responsive elements tagged with a SEAP reporter. In 10.5 day limb cells, gas1 overexpression had little effect on Ap-1, NFkappaB, and c-myc activities. In contrast, gas1 overexpression in 12.5 day limb cells enhanced AP-1 response while it inhibited NFkappaB and c-myc activities. These responses were directly associated with the ability of gas1 to induce growth arrest in embryonic limb cells. In the 12.5 day hindlimb, gas1 was found strongly expressed in the interdigital tissues. We overexpressed gas1 in these tissues and discovered that it promoted interdigital cell death. Our in situ hybridization studies of limb sections and micromass cultures revealed that, during the early stages of chondrogenesis, only cells surrounding the chondrogenic condensations expressed gas1. The gene was only expressed by chondrocytes after the cartilage started to differentiate. To understand the function of gas1 in chondrogenesis, we overexpressed the gene in limb micromass cultures. It was found that cells overexpressing gas1/GFP could not participate in cartilage formation, unlike cells that just express the GFP reporter. We speculated that the reason gas1 was expressed outside the chondrogenic nodules was to restrict cells from being recruited into the nodules and thereby defining the boundary between chondrogenic and nonchondrogenic forming regions."

Several cells were sampled in LSJL so it's likely that the non-chondrogenic cells were the ones expressing Gas1.

"product of gas1 is located in the cell membrane and that it contains a large extracellular domain. This domain contains an arginine– glycine–aspartic acid sequence (RGD), which suggests that it could interact with integrin-type molecules. Therefore, gas1 could be involved in cell– cell and cell–matrix interactions. It is possible that cells expressing gas1 are more anchored to the extracellular matrix and thereby inhibited from participating in chondrogenesis."